Ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (TUDCA) are anti-apoptotic molecules with protective effects against several neurodegenerative disorders such as Alzheimer's and Parkinson's diseases as well as against acute kidney injury. Both UDCA and TUDCA block the initiating event of the apoptotic process, in part, through stabilizing the mitochondrial membrane potential, a mechanism that enhances the integrity of the mitochondria. Enhanced mitochondrial integrity abolishes the release of several mitochondrial proteins such as cytochrome C into the cytosol, thereby preventing the onset of apoptosis. Further, UDCA and TUDCA upregulate several pathways that function synergistically with their anti-apoptotic properties.
The kinetic deuterium isotope effect (KDIE) is a function of enhanced carbon-deuterium (C-D) bond strength over the carbon-hydrogen (C—H) bond, often several-fold. Substitution of the C—H by the C-D bond significantly decreases breakage, thereby increasing the resident time of the molecule in the body. Therefore, substituting one or more of the carbons with deuterium significantly increases the metabolic clearance time. An added benefit of the KDIE is the possibility of using lower dosages to derive the same pharmacological effect. The C-D bond is twice as strong as the C—H bond by virtue of a two-fold higher mass of deuterium over hydrogen. Hence, the reaction rate of the C-D bond breakage is significantly slower than that of the C—H bond breakage.